A molecular pathway for light-dependent photoreceptor apoptosis in Drosophila
A molecular pathway for light-dependent photoreceptor apoptosis in Drosophila
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DOI：
10.1016/s0896-6273(00)00092-1
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发表时间：
2000-10-01
期刊：
影响因子：
16.2
通讯作者：
Ranganathan, R
中科院分区：
文献类型：
--
作者：
Kiselev, A;Socolich, M;Ranganathan, R
光诱导的感光细胞凋亡发生在许多形式的遗传性视网膜变性中，导致脊椎动物和无脊椎动物的失明。虽然在几个感光细胞信号蛋白的突变已牵连在触发这一过程中，有关视紫红质光激活感光细胞死亡的分子事件还不清楚。在这里，我们发现了一个途径，通过激活视紫红质在果蝇介导的细胞凋亡，通过G蛋白的独立机制。这一过程涉及形成膜复合物的磷酸化，激活视紫红质和其抑制蛋白arrestin，和随后的网格蛋白依赖性内吞这些复合物进入细胞质室在一起，这些数据定义的促凋亡分子在果蝇光感受器，并表明一种新的信号通路光激活视紫红质分子在控制感光细胞的活力。
Light-induced photoreceptor apoptosis occurs in many forms of inherited retinal degeneration resulting in blindness in both vertebrates and invertebrates. Though mutations in several photoreceptor signaling proteins have been implicated in triggering this process, the molecular events relating light activation of rhodopsin to photoreceptor death are yet unclear. Here, we uncover a pathway by which activation of rhodopsin in Drosophila mediates apoptosis through a G protein-independent mechanism. This process involves the formation of membrane complexes of phosphorylated, activated rhodopsin and its inhibitory protein arrestin, and subsequent clathrin-dependent endocytosis of these complexes into a cytoplasmic compartment Together, these data define the proapoptotic molecules in Drosophila photoreceptors and indicate a novel signaling pathway for light-activated rhodopsin molecules in control of photoreceptor viability.